CANCER CONTROL TRIAL BY C-MYC ANTISENSE DNA

Northern印迹杂交显示85%的结直肠癌组织中有c-myc基因的信使RNA过表达，而max基因无过表达。在我们的研究中，翻译起始基因的反义DNA不能抑制人结直肠癌来源的c-myc mRNA过表达的Colo-320 DM细胞的生长。因此，我们研究了细胞周期蛋白依赖性激酶(CDK)抑制剂CIP1/WAF1基因在结直肠癌中的表达，以寻找更重要的细胞生长基因。16例肿瘤组织中的表达均低于相应的非肿瘤组织。并通过相应DNA的聚合酶链式反应-单链构象多态方法检测P53基因突变，共检出6例突变病例。与野生型P53相比，突变型P53的mRNA表达水平更低。这些结果表明，通过CIP1/WAF1基因调控有可能进行更有效的治疗

Northern blot hybridization revealed messenger RNA overexpression of c-myc gene in 85% colorectal carcinoma tissues, however, there was no overexpression for max gene. In our investigation, the antisense DNA for the translation starting locus could not depress cell growth of COLO-320 DM which derived from human colorectal cancer and had c-myc mRNA overexpression.Thereafter, we investigated the mRNA expression of CIP1/WAF1 gene which was cycline dependent kinase (CDK) inhibitor in colorectal carcinoma to detect more important cell growth genes. The expression in tumor tissues were depressed in all 16 case compared with the correspondent nontumor tissues. We also detect the p53 gene mutation through the PCR-SSCP method for the correpondent DNA.We could identified 6 mutation cases in 16 cases. These mutant cases indicated the more depressed mRNA expression compared with wilds p53 cases. These result indicated that there could be the possibility for more useful therapy through CIP1/WAF1 gene control